Susceptibility of DPOAEs to sound overexposure in inbred mice with AHL.

The notion that three inbred strains of mice, i.e., C57BL/6J (C57), BALB/cByJ (BALB), and WB/ReJ (WB), which exhibit differential rates of age-related hearing loss (AHL), may also exhibit differential susceptibility to noise-induced hearing loss was tested by comparing the effects of sound overexposure on these strains. The aftereffects of noise overstimulation on the distortion-product otoacoustic emissions (DPOAEs) of these three strains were compared and contrasted to those for the CBA/CaJ (CBA) strain, which does not show changes in hearing threshold sensitivity up to 15 months of age. Two cohorts of mice, one at 2.5 and the other at 6 months of age, were first exposed to a tonal overstimulation paradigm, were allowed to recover, and then were later re-exposed to an octave band noise (OBN), at 3 or 7 months of age, respectively. The two sound exposure episodes were designed to produce either a temporary (tonal exposure) or permanent (OBN exposure) reduction in the levels of the 2f1 - f2 DPOAE in the WB strain, which exhibited the fastest rate of AHL. Although the tonal paradigm resulted in a temporary decrease in DPOAE levels for all strains at both ages, the 2.5-month BALBs showed the greatest susceptibility to this overexposure, while the 2.5-month WBs exhibited the least effects on DPOAEs. At the older age of 6 months, tonal overexposure produced essentially the same reduction in DPOAE levels for all four strains. In addition, there were no differences noted between CBAs and C57s, at either of the two ages. The OBN paradigm resulted in a permanent decrease in DPOAE levels in all the strains exhibiting early AHL, i.e., the C57, BALB, and WB mice, for frequencies about one-half to an octave higher than the exposure frequency, regardless of age. In contrast, the CBA strain was not significantly affected by the OBN overexposure.

Suppression and enhancement of distortion-product otoacoustic emissions by interference tones above f(2). I. Basic findings in rabbits.

The present study measured interference-response areas (IRAs) for distortion-product otoacoustic emissions (DPOAEs) at 2f(1)-f(2), 3f(1)-2f(2), and 2f(2)-f(1). The IRAs were obtained in either awake or anesthetized rabbits, or in anesthetized guinea pigs and mice, by sweeping the frequencies and levels of an interference tone (IT) around a set of f(1) and f(2) primary tones, at several fixed frequencies and levels, while plotting the effects of the IT on DPOAE level. An unexpected outcome was the occurrence of regions of suppression and/or enhancement of DPOAE level when the IT was at a frequency slightly less than to more than an octave above f(2). The IRA of the 2f(1)-f(2) DPOAE typically displayed a high-frequency (HF) lobe of suppression, while the 2f(2)-f(1) emission often exhibited considerable amounts of enhancement. Moreover, for the 2f(2)-f(1) DPOAE, when enhancement was absent, its IRA usually tuned to a region above f(2). Whether or not suppression/enhancement was observed depended upon primary-tone level and frequency separation, as well as on the relative levels of the two primaries. Various physiological manipulations involving anesthesia, eighth-nerve section, diuretic administration, or pure-tone overstimulation showed that these phenomena were of cochlear origin, and were not dependent upon the acoustic reflex or cochlear-efferent activity. The aftereffects of applying diuretics or over-exposures revealed that suppression/enhancement required the presence of sensitive, low-level DPOAE-generator sources. Additionally, suppression/enhancement were general effects in that, in addition to rabbits, they were also observed in mice and guinea pigs. Further, corresponding plots of DPOAE phase often revealed areas of differing phase change in the vicinity of the primary tones as compared to regions above f(2). These findings, along with the effects of tonal exposures designed to fatigue regions above f(2), and instances in which DPOAE level was dependent upon the amount of suppression/enhancement, suggested that the interactions of two DPOAE-generator sources contributed, in some manner, to these phenomena.

Locus of generation for the 2f1-f2 vs 2f2-f1 distortion-product otoacoustic emissions in normal-hearing humans revealed by suppression tuning, onset latencies, and amplitude correlations.

The present study used distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs), DPOAE onset latencies (OLs), and DPOAE amplitude correlations to investigate the locus of generation of the 2f1-f2 DPOAE versus the 2f2-f1 DPOAE in humans. The results of the tuning study revealed that, for the 2f1-f2 DPOAE, the tips of the STCs tuned consistently below the geometric-mean (GM) frequency of the primary tones. In contrast, for the 2f2-f1 DPOAE, STCs tuned above the GM of the primaries, with 50% of the tip frequencies at, or above, the 2f2-f1 frequency place. When the average ratio of the 2f2-f1 to the 2f1-f2 tip frequencies was computed, a factor of 1.44 provided an estimate of the frequency shift needed to align the two DPOAE generation sites. Other results showed that OLs for the 2f2-f1 DPOAE were uniformly shorter than those for the 2f1-f2, with differences at the low frequencies amounting to as much as 6-7 ms. Further, for both DPOAEs, curves describing latency decreases as a function of increasing GM frequencies were best fit by power functions. Shifting the GM frequency producing the 2f2-f1 DPOAE by a factor of 1.6 caused the latency distributions for both DPOAEs to overlap thus resulting in a single function that described cochlear delay as a function of GM frequency. Finally, for each GM frequency in the DP-gram, sliding correlations from 108 normal ears were performed on both DPOAEs by holding the primaries producing the 2f1-f2 DPOAE constant, while all 2f2-f1 DPOAE amplitudes were successively correlated with the 2f1-f2 amplitudes. This procedure demonstrated that, for a given GM frequency producing the 2f1-f2, the correlations between the two DPOAEs peaked when the primaries of the 2f2-f1 were at a GM frequency that positioned the 2f2-f1 frequency place near the GM of the primaries that produced the 2f1-f2 DPOAE. As a whole, the above findings strongly suggest that the 2f2-f1 DPOAE in humans is generated basal to the primary-tone place on the basilar membrane.

Effects of ear-canal standing waves on measurements of distortion-product otoacoustic emissions.

At frequencies above 3 kHz, standing waves in the ear canal complicate calibration of stimulus sound-pressure levels (SPLs) for measurements of distortion-product otoacoustic emissions (DPOAEs). In the literature, two stimulus-presentation strategies have been used for DPOAE measurements. In the "in-the-ear adjustment" strategy, the voltage command to the speakers is adjusted to maintain a constant stimulus SPL across frequency at the DPOAE-measurement microphone. In the "iso-voltage" strategy, the voltage presented to the speakers is held constant across frequency, on the basis of the assumption that the frequency response of the speakers is approximately flat at the eardrum in the average human ear canal. Because of standing-wave effects, there are large, systematic but idiosyncratic differences of stimulus SPL between the two strategies. DPOAE-versus-frequency functions ("DPOAE audiograms") obtained using both stimulus-presentation strategies in the same ears are presented. The differences of stimulus SPL between the two strategies, and the associated differences of DPOAE amplitude, are described and quantified. Around frequencies of standing-wave minima at the DPOAE probe, the in-the-ear adjustment strategy resulted in smaller DPOAEs at high L1 = L2, but much larger DPOAEs at low L1 = L2, than did the iso-voltage strategy. For any L1, the DPOAE-amplitude differences between the two strategies varied systematically with L1-L2. At the stimulus levels used to construct previously published population norms for clinical applications (i.e., L1 > or = 65 dB SPL), there are only small differences of mean DPOAE amplitudes, and of the standard deviations of these means, between the two strategies.

Time-windowing of click-evoked otoacoustic emissions to increase signal-to-noise ratio.

OBJECTIVE: To investigate the effects of decreasing the response-window duration on the signal-to-noise ratio (S/N) of click-evoked otoacoustic emissions (CEOAEs). DESIGN: The ILO88 (Otodynamics, Ltd.) was used to measure CEOAEs from 149 normal adult ears, and 75 adult ears with high-frequency sensorineural hearing loss. Data were collected using the default response window of 2.5 to 20.5 msec post-click. Each response was rewindowed, post-hoc, from 2.5 to 7.5 msec, 2.5 to 9 msec, 7.75 to 14.25 msec, and 13 to 19.5 msec post-click. For each window, spectra of the CEOAE and of the background noise were determined. The S/N was estimated by subtracting the noise level from the CEOAE amplitude. RESULTS: The 13- to 19.5-msec window contained little CEOAE energy relative to earlier windows. Relative to the 2.5- to 20.5-msec window, the 2.5- to 7.5- and 2.5- to 9-msec windows reduced noise levels more than CEOAE amplitudes, yielding increased S/N, and greater "reproducibility" values. The increased S/N of the 2.5- to 7.5- and 2.5- to 9-msec windows allowed measurement of greater CEOAE-amplitude reductions in the impaired ears relative to the normal ears. With short-duration windows, click-presentation rate could be increased, allowing more responses to be averaged in a given time, thus further decreasing noise levels. Although click rate was not varied in the present study, the decrease of noise levels is predictable. Accounting for this factor, it is expected that a specified S/N would be obtained about five times faster using the 2.5- to 7.5-msec window with a 7.5-msec interstimulus interval, than when using the default window. CONCLUSIONS: Decreasing the response-window duration substantially increases the measurement efficiency of CEOAEs in adults, and thus may enhance clinical-test performance.

Sensitivity of distortion-product otoacoustic emissions in humans to tonal over-exposure: time course of recovery and effects of lowering L2.

An important concern of industrial hearing-conservation programs is detecting the onset of noise-induced hearing loss. If it can be shown that otoacoustic emissions are sufficiently sensitive to reliably detect auditory fatigue and the permanent hearing loss that eventually develops, they could become an important part of the hearing-conservation test battery. The present study in humans was designed to examine the influence of overall primary-tone level and the effects of lowering the f2 primary on the sensitivity of distortion-product otoacoustic emissions (DPOAEs) to acoustic overstimulation. One ear from each of 14 subjects with normal hearing was exposed to a 105-dB SPL pure tone at 2.8 kHz for 3 min using a protocol consisting of distinct pre-exposure, exposure, and post-exposure periods. As a quantitative index of the functional status of the outer hair cells, 2f1-f2 DPOAEs were monitored systematically over time using four stimulus-test conditions consisting of either one of two levels of equilevel primary tones, or one of two levels of offset primaries, with L2 set 25 dB lower than L1. The overall finding was that the DPOAE protocol incorporating both the lowest level of stimulation and an f2-primary tone that was 25 dB below the level of the f1 stimulus [i.e., L1 (55 dB SPL) - L2 (30 dB SPL) = 25 dB] was most sensitive to the exposure effects. The results establish that DPOAEs elicited with unequal, in contrast to equal-level primaries, have comparable signal-to-noise ratios, but are considerably more sensitive to reductions in emission levels induced by exposure to short-lasting, moderately intense tones. The recovery of DPOAE amplitudes over the first 15 min post-exposure appeared to be roughly linear in log time and, in many cases, could be closely approximated by fitting a logarithmic curve to the post-exposure data. From these functions, the initial amount of loss (y-intercept) and the slope of recovery were identified as potential measures of vulnerability to acoustic exposure in that these variables appeared to be related to the susceptibility of some of the subjects, who also participated in a subsequent experiment on the behavioral effects of the exposure stimulus. Finally, compared to behaviorally measured temporary threshold shift (TTS), the time course of the recovery for DPOAEs was very similar, suggesting that, with the appropriate parameters, DPOAEs can be as sensitive to TTS as routine pure-tone audiometry.

The influence of noise on the measured amplitudes of distortion-product otoacoustic emissions.

This paper describes the influence of noise on the measured amplitudes of tonal signals, as determined using narrowband spectral analysis, that is, the technique typically used to measure distortion-product otoacoustic emissions (DPOAEs). At small signal-to-noise ratios, background noise results in overestimation of DPOAE amplitude and, thus, substantially influences the measured properties of the low-level portions of DPOAE-growth functions, in particular the apparent slope of the functions in this region. It is shown that, because of the influence of noise, the algorithm for the objective estimation of detection thresholds of DPOAEs, and of the slopes of DPOAE-growth functions, described by Nelson and Kimberley (1992), will tend to underestimate these values. This systematic underestimation is presumably the reason why many of the DPOAE-detection thresholds and growth slopes presented in that study were considerably lower than those reported in previous studies using similar measuring equipment and paradigms but different detection-threshold and growth-slope estimation techniques. In the present paper, a simple equation allowing an estimated correction for the effects of noise on measured DPOAE amplitudes is presented. Finally, an alternative strategy for the estimation of DPOAE thresholds, one that is less prone to the influence of noise, is suggested.

Distortion-product emissions in rabbit: I. Altered susceptibility to repeated pure-tone exposures.

An important issue in understanding the development of noise-induced hearing loss is whether prior acoustic overstimulation alters the susceptibility of the cochlea to further damage. The present work was designed to establish a model of activity-dependent changes in the susceptibility of the cochlea to acoustic overstimulation by regularly exposing the ear to a low-frequency pure tone. As a quantitative index of cochlear function, 2f1-f2 distortion-product otoacoustic emissions (DPOAEs) were monitored systematically over time in three groups of rabbits, with each group experiencing a unique paradigm that incorporated repeated exposure to the low-frequency tone. Common to each rabbit's exposure protocol was that a given experimental session consisted of two exposure episodes, separated by a 40-min period. Experimental sessions were repeated three times, with 2- to 3-day recovery periods interposed between sessions. The rate of decrement in DPOAE amplitude over a prescribed time period was utilized as a measure of susceptibility to the acoustic trauma. The overall results indicated that ears were more susceptible to exposure 40 mins after the first exposure of a session than they were initially. A series of control experiments indicated that the robustness of the acoustic middle-ear reflex (AMR) did not change between the exposure episodes. Consequently, changes in the AMR could not account for the increased susceptibility seen following the first exposure. However, in awake rabbits with stronger AMRs, higher pure-tone exposure levels were needed to produce increased susceptibility to the second exposure. After 2-3 days of intersession recovery, susceptibility to the effects of excessive sound returned close to its original baseline level. The outcome of these studies demonstrated a reduced capacity for the ear to resist the harmful effects of exposure to a moderately intense tone, which was repeated twice over a brief 40-min period, but little change in susceptibility when identical exposures were repeated over longer intersession intervals of several days.

Clinical testing of distortion-product otoacoustic emissions.

Otoacoustic emissions have great promise for use in clinical tests of the functional status of outer hair cells, which represent cochlear structures that make a major contribution to the hearing process. A substantial literature is available concerning the evaluation of outer hair cell function by transiently evoked otoacoustic emissions. However, relatively little attention has been focused on the benefits of testing with distortion-product otoacoustic emissions. The purpose of this presentation is to provide knowledge of the principal advantages offered by distortion-product emissions testing.

Spontaneous otoacoustic emissions in different racial groups.

To determine if there are racial differences in the prevalence of spontaneous otoacoustic emissions (SOAEs), both ears of 20 Negro, 20 Asian and 20 Caucasian subjects were examined for the presence of SOAEs. Within each racial group, equal numbers of normally hearing males and females were tested. Significant differences in the occurrence of SOAEs were found between the three racial groups, with Negroes expressing more SOAEs than Caucasians, and Asians demonstrating an intermediate number of these emissions. In support of previous observations, more emissions were recorded from female than from male ears, and a significant correlation of the number of emissions in the two ears of an individual was also noted.

Evidence for two discrete sources of 2f1-f2 distortion-product otoacoustic emission in rabbit. II: Differential physiological vulnerability.

In a previous report, it was shown that, in normal rabbit ears, the amplitude and phase of 2f1-f2 distortion-product otoacoustic emissions (DPOAEs) elicited by low-level (< 60-70 dB SPL) stimuli display a differential dependence on stimulus parameters to those evoked by high-level (> 60-70 dB SPL) stimuli, indicating differences in the underlying generation mechanisms. In the present study, the physiological vulnerability of DPOAEs in each of the two 2f1-f2 DPOAE-response regions identified on the basis of differential parametric properties, was characterized. Thus emissions evoked using stimulus levels from 45-75 dB SPL were measured over time upon: (1) induction of lethal anoxia, (2) acute injection of ethacrynic acid, and (3) acute injection of ethacrynic acid 2 h after a single administration of gentamicin. The DPOAEs evoked by low-level stimuli (45 dB SPL) were abolished within 3-4 min of induction of anoxia, whereas DPOAEs evoked by high-level stimuli (75 dB SPL) were unchanged in this period. The high-level emissions decreased with a complex time course postmortem, and demonstrated behaviors, including evidence of susceptibility to fatigue, suggesting a dependence upon a cochlear energy supply. Low-level DPOAEs could be temporarily abolished, with complete recovery, by an acute administration of ethacrynic acid that had little effect on high-level DPOAEs. Treatment with the gentamicin and ethacrynic-acid combination, which would be expected to produce widespread hair-cell damage, eliminated low-level DPOAEs, and greatly reduced high-level emissions. In combination with previously published data, these findings strongly suggest that low- and high-level 2f1-f2 DPOAEs arise from discrete sources. The data are consistent with the proposal that the low-level DPOAE source is an active, micromechanical process, but suggest that the proposed origin of high-level DPOAEs exclusively in the passive macromechanics of the cochlear partition may be incorrect. The elimination of both low- and high-level DPOAEs revealed the presence of a third, residual 2f1-f2 DPOAE component, approximately 75-80 dB below the stimulus-tone levels, that may reflect the true passive-distortion response of the cochlea.

Acoustic-distortion products: separation of sensory from neural dysfunction in sensorineural hearing loss in human beings and rabbits.

Because distortion-product otoacoustic emissions (DPOAEs) provide a noninvasive measure of outer hair-cell (OHC) activity, they should provide a unique and sensitive indicator of the effects of agents that damage hearing. Using DPOAE methods, the present study was designed to assess the relative contributions of the cochlea's outer hair cells to some common sensorineural diseases, including Meniere's disease, acoustic neuroma, and noise-induced, hereditary, and sudden idiopathic sensorineural hearing loss. Parallel evaluations of DPOAEs were performed under essentially identical conditions in rabbit models of several of the human disorders, including noise-induced hearing loss, endolymphatic hydrops, and cochlear neurectomy. Animal studies were performed to assess the proficiency of DPOAEs to track a developing sensorineural deficit as well as to compare patterns of DPOAE dysfunction between clinical and experimental forms of peripheral hearing loss. Detailed measures of DPOAEs were collected in the stimulus-frequency and intensity domains as "audiograms" and response/growth or input/output functions, respectively. The outcome of analyses of both human beings and animals supported the notion that DPOAE testing is sensitive to sensory-cell disease. Thus, in combination with conventional audiometry, DPOAE measures permit a distinction between the relative contribution sensory and neural components of the cochlea make to hearing deficits.

Effects of the crossed acoustic reflex on distortion-product otoacoustic emissions in awake rabbits.

Recent studies in anesthetized cats suggest that contralateral-sound stimulation acts to suppress ipsilateral neural responses via the medial olivocochlear-efferent system. Activation of this descending efferent pathway presumably influences ipsilateral outer hair cell motility and, thus, cochlear micromechanics, resulting in reduced input to auditory-nerve fibers. The principal aim of the present study was to determine if contralateral-sound stimuli influence the generation of ipsilateral distortion-product otoacoustic emissions, in the ears of awake rabbits. The results showed no effects of contralateral stimuli on these emissions that could not be attributed to the crossed acoustic middle-ear reflex. The findings further indicate that distortion-product otoacoustic emission amplitudes over a wide range of frequencies can be dramatically reduced when the middle-ear reflex is activated.

Distortion product emissions in humans. II. Relations to acoustic immittance and stimulus frequency and spontaneous otoacoustic emissions in normally hearing subjects.

Multifrequency and multicomponent evaluations of aural acoustic immittance, including tympanometry and acoustic reflex testing, were performed on 44 normal ears to examine the influence of middle ear functioning on the generation and detection of distortion product otoacoustic emissions (DPEs). In the same ears, the prevalence and parametric features of spontaneous and stimulus frequency emissions were also assessed so that their relationship to the detection "thresholds" and amplitudes of corresponding DPEs could be determined. The general outcome was that none of the examined features of acoustic immittance provided an explanation for the discrete, low-amplitude DPE regions observed in about one third of normal ears. Moreover, the presence of typical spontaneous and stimulus frequency emissions in these same "irregular" ears indicated that emission generation and reverse cochlear transmission were also operating normally within these regions of reduced DPEs. Consequently, other, as yet undetermined influences appear to contribute to the DPE variability noted in some ears. Finally, the simultaneous presence of stimulus frequency emissions, but not spontaneous emissions, appeared to reduce the detection "thresholds" and increase the amplitudes of low-frequency DPEs.

Distortion product emissions in humans. I. Basic properties in normally hearing subjects.

Distortion product otoacoustic emissions (DPEs) at the 2f1-f2 frequency were recorded from 44 normal ears in response to equilevel primary tones. Detailed testing included the recording of DPE "audiograms" in 100-Hz steps from 1 to 8 kHz at three primary-tone levels (65, 75, and 85 dB sound pressure level [SPL]). In addition, response-growth or input-output (I/O) functions depicting the relationship of the amplitudes of DPEs to primary-tone levels, ranging from 25 to 85 dB SPL in 5-dB steps, were also tested for 11 frequencies distributed at quarter-octave intervals over the identical frequency range. The average DPE "audiogram" illustrating the frequency response of these emissions demonstrated a bilobed contour having a low-frequency maximum at approximately 1.5 kHz and a high-frequency peak that plateaued at about 5.5 kHz. The two maximum regions were separated by a minimum around 2.5 kHz. Depending on the frequency region, the average I/O functions exhibited detection "thresholds" at 3 dB above the noise floor at primary levels between 35 and 45 dB sound pressure level. The dynamic range of the emitted response between detection "threshold" and maximum amplitude varied over a 40-dB extent of the stimulus-level dimension. Approximately one third of the ears exhibited irregular DPE "audiograms" in which emitted responses were significantly reduced in restricted regions tested by low, medium, or high frequencies. When the 44 ears were separated into two groups representing more-normal and less-normal responses, the irregular "normal" ears demonstrated increased variability, especially in high-frequency regions. Mean age did not explain the differences noted between the two types of normally hearing subjects. However, across ears, DPE amplitudes and "thresholds" for the highest frequencies tested were correlated significantly with age in that the oldest individuals showed higher "thresholds" and lower amplitudes.

Spontaneous otoacoustic emissions in a nonhuman primate. I. Basic features and relations to other emissions.

Otoacoustic emissions in both ears of a rhesus monkey exhibiting stable spontaneous emissions (SOEs) were monitored over a 1-year period. The amplitudes and frequencies of both SOEs and stimulus-frequency emissions (SFEs) were routinely recorded, while transiently evoked (EOE) and distortion-product emissions (DPEs), at the frequency 2f1-f2, were occasionally examined. Between evaluation sessions, both the frequencies and amplitudes of SFEs remained relatively stable in both ears, while the frequencies and amplitudes of SOEs were less constant. Isosuppression contours for SOEs, plotted as a function of frequency and level of tonal maskers, revealed sharp tuning consistent with normal frequency selectivity. Detailed analyses of long-term measurements showed that SOEs occurred most frequently at the peaks of the SFE response. A regular frequency spacing between neighboring amplitude maxima and minima of the SFEs was consistent with the notion that this particular emitted response may result from a periodic disruption of the orderly pattern of sensory cells along the organ of Corti. Intramuscular administration of aspirin abolished SOE and SFE responses, while DPEs remained relatively unchanged suggesting the involvement of separate mechanisms in the generation of different emissions.

Otoacoustic emissions in ears with hearing loss.

Fifty ears of 37 patients demonstrating several common types of hearing impairment were examined for the presence of spontaneous and evoked otoacoustic emissions to investigate the relationship of acoustic emissions to hearing pathology. Of the 50 ears, 44 exhibited various degrees of sensorineural hearing loss. Evoked otoacoustic emissions to clicks were detected in 34 of 35 sensorineural hearing loss ears with a subjective click threshold less than 55 dB SPL (25 dB nHL). None of nine ears with sensorineural hearing impairment and a subjective click threshold greater than 55 dB SPL demonstrated click-evoked emissions. Spectral analyses revealed that the constituent frequency components of evoked emissions were always within the frequency range where audiometric thresholds were less than 35 dB HL, and in the majority (94%) of cases, thresholds were less than 25 dB HL. In ears with relatively well-preserved hearing within the frequency range of click or 1.5-kHz toneburst stimuli, the basic features of evoked emissions were similar to those described for normal ears. Similarly, for ears demonstrating spontaneous otoacoustic emissions, estimated audiometric thresholds at the emitted frequencies were always less than 20 dB HL. The influence of the type of otologic pathology on acoustic emissions was studied in a subset of ears exhibiting typical high-frequency hearing losses. Ears with a noise-induced impairment showed a significant reduction in the incidence of both spontaneous emissions and spectral peaks in evoked emissions that was not evident in ears with similar patterns of hearing loss caused by other factors.

Spontaneous, click-, and toneburst-evoked otoacoustic emissions from normal ears.

Evoked and spontaneous otoacoustic emissions were recorded bilaterally in a group of normal subjects (n = 14) using clicks and tonebursts at four frequencies (0.5, 1, 1.5, and 3 kHz). All ears (n = 28) demonstrated evoked emissions, but not to every stimulus type. The 0.5-kHz toneburst evoked emissions in only 10 (36%) ears, the 1.5-kHz toneburst in all ears, and the remaining stimuli in at least 80% of ears. Two distinct patterns of evoked emissions were identified. Five (18%) ears showed short, broadband click-evoked emissions lasting less than 20 ms after stimulus onset. In these ears, toneburst-evoked emissions were often more prominent than click-evoked emissions and no spontaneous emissions were detected. Twenty-three (82%) ears showed click-evoked emissions lasting longer than 20 ms poststimulus onset. Spectral analysis of these emissions demonstrated several (2-10) narrow frequency peaks. Highly similar peaks were present in the spectra of toneburst-evoked emissions within the range of toneburst spectra. Spontaneous emissions were recorded in 12 of the 23 ears. In these ears, at the frequencies of spontaneous emissions, prominent peaks in both click- and toneburst-evoked emission spectra were always present. Otoacoustic emission characteristics correlated significantly between the ears of individual subjects inferring that a symmetrical cochlear mechanism generates otoacoustic emissions.